Daniel H. Silverman

About

Dr. Daniel H. Silverman is a Clinical Professor in the Department of Molecular and Medical Pharmacology at UCLA and serves as the Head of the Neuronuclear Imaging Section within the Ahmanson Biological Imaging Division at UCLA Medical Center. He is also a member of the Cancer Molecular Imaging, Nanotechnology and Theranostics program. Dr. Silverman holds an MD from Ohio State University College of Medicine and a PhD from Harvard University. He completed his internship and residency in Internal Medicine as well as a fellowship in Nuclear Medicine at UCLA School of Medicine. He is board certified in both Nuclear Medicine and Internal Medicine. Dr. Silverman's research program focuses on two major goals: exploring the interactions and neurologic bases of memory, mood, and pain perception in the living human brain, particularly in both normal and disordered states such as dementia, depression, and chronic pain syndromes; and developing noninvasive methodologies to optimize the management of breast and colorectal cancers. These objectives are connected through the use of low-level radioactive biochemicals to characterize and map biological processes in the human body that are relevant to patients seen in nuclear and internal medicine. His research extensively applies positron emission tomography (PET) to study molecular processes and human behaviors, spanning from biochemical work in vitro to clinical monitoring and treatment of patients in the Ahmanson Biological Imaging Clinic.

Research topics

• Medicine
• Neuroscience
• Psychology
• Pathology
• Biology
• Internal medicine
• Artificial Intelligence
• Machine Learning
• Oncology
• Computer Science

Selected publications

• Spread of pathological tau proteins through communicating neurons in human Alzheimer’s disease

  Nature Communications · 2020 · 532 citations

  Tau is a hallmark pathology of Alzheimer's disease, and animal models have suggested that tau spreads from cell to cell through neuronal connections, facilitated by β-amyloid (Aβ). We test this hypothesis in humans using an epidemic spreading model (ESM) to simulate tau spread, and compare these simulations to observed patterns measured using tau-PET in 312 individuals along Alzheimer's disease continuum. Up to 70% of the variance in the overall spatial pattern of tau can be explained by our mod…

  DOI

• Functional brain architecture is associated with the rate of tau accumulation in Alzheimer’s disease

  Nature Communications · 2020 · 338 citations

  In Alzheimer's diseases (AD), tau pathology is strongly associated with cognitive decline. Preclinical evidence suggests that tau spreads across connected neurons in an activity-dependent manner. Supporting this, cross-sectional AD studies show that tau deposition patterns resemble functional brain networks. However, whether higher functional connectivity is associated with higher rates of tau accumulation is unclear. Here, we combine resting-state fMRI with longitudinal tau-PET in two independe…

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• Challenges and Opportunities with Causal Discovery Algorithms: Application to Alzheimer’s Pathophysiology

  Scientific Reports · 2020 · 133 citations

  Causal Structure Discovery (CSD) is the problem of identifying causal relationships from large quantities of data through computational methods. With the limited ability of traditional association-based computational methods to discover causal relationships, CSD methodologies are gaining popularity. The goal of the study was to systematically examine whether (i) CSD methods can discover the known causal relationships from observational clinical data and (ii) to offer guidance to accurately disco…

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• Anatomically interpretable deep learning of brain age captures domain-specific cognitive impairment

  Proceedings of the National Academy of Sciences · 2023 · 116 citations

  = 359). In individuals with MCI (54% of whom were diagnosed with dementia within 10.9 y from MRI acquisition), BA is significantly better than CA in capturing dementia symptom severity, functional disability, and executive function. Profiles of sex dimorphism and lateralization in brain aging also map onto patterns of neuroanatomic change that reflect cognitive decline. Significant associations between BA and neurocognitive measures suggest that the proposed framework can map, systematically, th…

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• Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer’s amyloid, tau and FDG PET status

  Translational Psychiatry · 2021 · 68 citations

  Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. We aimed to evaluate whether it could serve as a marker for Alzheimer's pathology in the brain. A total of 1189 participants with plasma p-tau181 and PET data of amyloid, tau or FDG PET were included from ADNI. Cross-sectional relationships of plasma p-tau181 with PET biomarkers were tested. Longitudinally, we further investigated whethe…

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Recent grants

• NIH Grant R21NS071385

  NIH · $424k · 2014

• NIH Grant R21MH064679

  NIH · $305k · 2005

Frequent coauthors

• John C. Morris

  Washington University in St. Louis

  198 shared

• Andrew J. Saykin

  Indiana University

  185 shared

• Clifford R. Jack

  WinnMed

  174 shared

• Adam Fleisher

  Eli Lilly (United States)

  174 shared

• Michael W. Weiner

  University of California, San Francisco

  167 shared

• Michael Donohue

  Janssen (United States)

  166 shared

• Robert C. Green

  Ariadne Diagnostics (United States)

  162 shared

• Chris Hosein

  Jewish General Hospital

  152 shared

Education

• Ph.D. in Biochemistry, Cellular and Molecular Biology, Neuroscience

  Johns Hopkins School of Medicine

  2018

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